tbuckley/cabot-search huggingface dataset:
A successful endoscopic pancreatic stone extraction in a patient with pancreatic divisum with cholangiojejunostomy reconstruction
Authors: Ping Yue, Man Yang, Yanxian Ren, Wenbo Meng, Xun Li
Journal: Endoscopy (2022)

A 21-year-old woman who previously underwent choledochojejunostomy during childhood was admitted with a 1-week history of worsening upper abdominal pain. She was diagnosed with acute pancreatitis, and magnetic resonance cholangiopancreatography (MRCP) revealed a pancreatic divisum with multiple stones in both dilated ventral and dorsal pancreatic ducts ([Fig. 1]).
An anti-CD98 antibody displaying pH-dependent Fc-mediated tumour-specific activity against multiple cancers in CD98-humanized mice
Authors: Xinxin Tian, Ximing Liu, Jingjin Ding, Fengchao Wang, Kailun Wang, Juan Liu, Zhizhong Wei, Xinyan Hao, Yulu Li, Xin Wei, Huixiang Zhang, Jianhua Sui
Journal: Nature Biomedical Engineering (2022)
Multiregion transcriptomic profiling of the primate brain reveals signatures of aging and the social environment
Authors: Kenneth L Chiou, Alex R DeCasien, Katherina P Rees, Camille Testard, Cailyn H Spurrell, Aishwarya A Gogate, Hannah A Pliner, Sébastien Tremblay, Arianne Mercer, Connor J Whalen, Josué E Negrón-Del Valle, Mareike C Janiak, Samuel E Bauman Surratt, Olga González, Nicole R Compo, Michala K Stock, Angelina V Ruiz-Lambides, Melween I Martínez, Melissa A Wilson, Amanda D Melin, Susan C Antón, Christopher S Walker, Jérôme Sallet, Jason M Newbern, Lea M Starita, Jay Shendure, James P Higham, Lauren J N Brent, Michael J Montague, Michael L Platt, Noah Snyder-Mackler
Journal: Nature Neuroscience (2022)
Effect of ECOG performance status on outcomes in patients with acute myeloid leukemia and other high-grade myeloid neoplasms
Authors: Gabrielle Paras, Megan Othus, Kelda Schonhoff, Carole Shaw, Mohamed Sorror, Anna B. Halpern, Jacob Appelbaum, Paul Hendrie, Roland B. Walter, Elihu H. Estey, Mary-Elizabeth M. Percival
Journal: Leukemia (2022)
Biological drivers of clinical phenotype in myelofibrosis
Authors: John Mascarenhas, Hélène F. E. Gleitz, Helen T. Chifotides, Claire N. Harrison, Srdan Verstovsek, Alessandro Maria Vannucchi, Raajit K. Rampal, Jean-Jacques Kiladjian, William Vainchenker, Ronald Hoffman, Rebekka K. Schneider, Alan F. List
Journal: Leukemia (2022)

Abstract Myelofibrosis (MF) is a myeloproliferative disorder that exhibits considerable biological and clinical heterogeneity. At the two ends of the disease spectrum are the myelodepletive or cytopenic phenotype and the myeloproliferative phenotype. The cytopenic phenotype has a high prevalence in primary MF (PMF) and is characterized by low blood counts. The myeloproliferative phenotype is typically associated with secondary MF (SMF), mild anemia, minimal need for transfusion support, and normal to mild thrombocytopenia. Differences in somatic driver mutations and allelic burden, as well as the acquisition of non-driver mutations further influences these phenotypic differences, prognosis, and response to therapies such as JAK2 inhibitors. The outcome of patients with the cytopenic phenotype are comparatively worse and frequently pose a challenge to treat given the inherent exacerbation of cytopenias. Recent data indicate that an innate immune deregulated state that hinges on the myddosome-IRAK-NFκB axis favors the cytopenic myelofibrosis phenotype and offers opportunity for novel treatment approaches. We will review the biological and clinical features of the MF disease spectrum and associated treatment considerations.
Changes in parental sleep from pregnancy to postpartum: A meta-analytic review of actigraphy studies
Authors: Leo Parsons, Abby Howes, Christopher A. Jones, Andrew D.R. Surtees
Journal: Sleep Medicine Reviews (2022)

Sleep changes in new parents are widely observed but there is no extant meta-analysis of changes to sleep parameters in this group. We completed a meta-analysis of changes in actigraphy-measured parent sleep between pregnancy and the end of the first year of a child's life. A search of six databases was completed. Following review using predetermined inclusion and exclusion criteria, 16 papers were left for review. Data were extracted, analysed and each paper was reviewed for methodological quality. Where possible, subgroup analysis was completed based on time since birth and location of the study, and meta-regression of parent age. Parents' total sleep time and sleep efficiency were shown to decrease following the birth of a child, with wake after sleep onset increasing. This change was most notably observed in the first four weeks after birth. Up to 16 weeks post-birth, differences were still apparent, but sleep parameters were beginning to return to pre-birth levels. New parents experience a significant change in multiple sleep parameters following the birth of a child. Future data collection, using best practice actigraphy measurement, reporting a broader range of variables and including fathers, as well as mothers, is warranted.
Systemic AAV9.BVES delivery ameliorates muscular dystrophy in a mouse model of LGMDR25
Authors: Haiwen Li, Peipei Wang, Ethan Hsu, Kelsey M. Pinckard, Kristin I. Stanford, Renzhi Han
Journal: Molecular Therapy (2022)

Limb-girdle muscular dystrophy type R25 (LGMDR25) is caused by recessive mutations in BVES encoding a cAMP-binding protein, characterized by progressive muscular dystrophy with deteriorating muscle function and impaired cardiac conduction in patients. There is currently no therapeutic treatment for LGMDR25 patients. Here we report the efficacy and safety of recombinant adeno-associated virus 9 (AAV9)-mediated systemic delivery of human BVES driven by a muscle-specific promoter MHCK7 (AAV9.BVES) in BVES-knockout (BVES-KO) mice. AAV9.BVES efficiently transduced the cardiac and skeletal muscle tissues when intraperitoneally injected into neonatal BVES-KO mice. AAV9.BVES dramatically improved body weight gain, muscle mass, muscle strength, and exercise performance in BVES-KO mice regardless of sex. AAV9.BVES also significantly ameliorated the histopathological features of muscular dystrophy. The heart rate reduction was also normalized in BVES-KO mice under exercise-induced stress following systemic AAV9.BVES delivery. Moreover, intravenous AAV9.BVES administration into adult BVES-KO mice after the disease onset also resulted in substantial improvement in body weight, muscle mass, muscle contractility, and stress-induced heart rhythm abnormality. No obvious toxicity was detected. Taken together, these results provide the proof-of-concept evidence to support the AAV9.BVES gene therapy for LGMDR25. Limb-girdle muscular dystrophy type R25 (LGMDR25) is caused by recessive mutations in BVES encoding a cAMP-binding protein, characterized by progressive muscular dystrophy with deteriorating muscle function and impaired cardiac conduction in patients. There is currently no therapeutic treatment for LGMDR25 patients. Here we report the efficacy and safety of recombinant adeno-associated virus 9 (AAV9)-mediated systemic delivery of human BVES driven by a muscle-specific promoter MHCK7 (AAV9.BVES) in BVES-knockout (BVES-KO) mice. AAV9.BVES efficiently transduced the cardiac and skeletal muscle tissues when intraperitoneally injected into neonatal BVES-KO mice. AAV9.BVES dramatically improved body weight gain, muscle mass, muscle strength, and exercise performance in BVES-KO mice regardless of sex. AAV9.BVES also significantly ameliorated the histopathological features of muscular dystrophy. The heart rate reduction was also normalized in BVES-KO mice under exercise-induced stress following systemic AAV9.BVES delivery. Moreover, intravenous AAV9.BVES administration into adult BVES-KO mice after the disease onset also resulted in substantial improvement in body weight, muscle mass, muscle contractility, and stress-induced heart rhythm abnormality. No obvious toxicity was detected. Taken together, these results provide the proof-of-concept evidence to support the AAV9.BVES gene therapy for LGMDR25.
Majority of cutaneous squamous cell carcinoma recurrences occur within 3 years after diagnosis: A dual-center retrospective cohort study
Authors: Thet Su Win, Fadi Murad, Allison T. Vidimos, Shlomo A. Koyfman, Timothy D. Smile, Chrysalyne Schmults, Emily Ruiz
Journal: Journal of the American Academy of Dermatology (2022)
RNA Structural Dynamics Modulate EGFR-TKI Resistance Through Controlling <i>YRDC</i> Translation in NSCLC Cells
Authors: Boyang Shi, Ke An, Yueqin Wang, Yuhan Fei, Caixia Guo, Qiangfeng Cliff Zhang, Yun-Gui Yang, Xin Tian, Quancheng Kan
Journal: Genomics Proteomics & Bioinformatics (2022)

Abstract Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) positively affect the initial control of non-small cell lung cancer (NSCLC). Rapidly acquired resistance to EGFR-TKIs is a major hurdle in successful treatment. However, the mechanisms that control the resistance of EGFR-TKIs remain largely unknown. RNA structures have widespread and crucial functions in many biological regulations; however, the functions of RNA structures in regulating cancer drug resistance remain unclear. Here, the psoralen analysis of RNA interactions and structures (PARIS) method is used to establish the higher-order RNA structure maps of EGFR-TKIs-resistant and -sensitive cells of NSCLC. Our results show that RNA structural regions are enriched in untranslated regions (UTRs) and correlate with translation efficiency (TE). Moreover, yrdC N 6 -threonylcarbamoyltransferase domain containing (YRDC) promotes resistance to EGFR-TKIs. RNA structure formation in YRDC 3′ UTR suppresses embryonic lethal abnormal vision-like 1 (ELAVL1) binding, leading to EGFR-TKI sensitivity by impairing YRDC translation. A potential therapeutic strategy for cancer treatment is provided using antisense oligonucleotide (ASO) to perturb the interaction between RNA and protein. Our study reveals an unprecedented mechanism through which the RNA structure switch modulates EGFR-TKI resistance by controlling YRDC mRNA translation in an ELAVL1-dependent manner.
Demographic and laboratory differences seen between acute generalized exanthematous pustulosis and drug reaction with eosinophilia and systemic symptoms: A cross-sectional analysis
Authors: Matthew A. Gallardo, Teja Mallela, Ty Gilkey, Sonia Himed, Trent D. Walker, Kelsey B. Nusbaum, Abraham Korman, John Trinidad, Catherine Chung, Benjamin H. Kaffenberger
Journal: Journal of the American Academy of Dermatology (2022)
Engineered extracellular vesicles for delivery of siRNA promoting targeted repair of traumatic spinal cord injury
Authors: Yuluo Rong, Zhuanghui Wang, Pengyu Tang, Jiaxing Wang, Chengyue Ji, Jie Chang, Yufeng Zhu, Wu Ye, Jianling Bai, Wei Liu, Guoyong Yin, Lipeng Yu, Xuhui Zhou, Weihua Cai
Journal: Bioactive Materials (2022)

Spinal cord injury (SCI) is a severe disease of the nervous system that causes irreparable damage and loss of function, for which no effective treatments are available to date. Engineered extracellular vesicles (EVs) carrying therapeutic molecules hold promise as an alternative SCI therapy depending on the specific functionalized EVs and the appropriate engineering strategy. In this study, we demonstrated the design of a drug delivery system of peptide CAQK-modified, siRNA-loaded EVs (C-EVs-siRNA) for SCI-targeted therapy. The peptide CAQK was anchored through a chemical modification to the membranes of EVs isolated from induced neural stem cells (iNSCs). CCL2-siRNA was then loaded into the EVs through electroporation. The modified EVs still maintained the basic properties of EVs and showed favorable targeting and therapeutic effects in vitro and in vivo. C-EVs-siRNA specifically delivered siRNA to the SCI region and was taken up by target cells. C-EVs-siRNA used the inherent anti-inflammatory and neuroreparative functions of iNSCs-derived EVs in synergy with the loaded siRNA, thus enhancing the therapeutic effect against SCI. The combination of targeted modified EVs and siRNA effectively regulated the microenvironmental disturbance after SCI, promoted the transformation of microglia/macrophages from M1 to M2 and limited the negative effects of the inflammatory response and neuronal injury on functional recovery in mice after SCI. Thus, engineered EVs are a potentially feasible and efficacious treatment for SCI, and may also be used to develop targeted treatments for other diseases.
Liquid exfoliation of ultrasmall zirconium carbide nanodots as a noninflammatory photothermal agent in the treatment of glioma
Authors: Dongdong Liu, Xingliang Dai, Wei Zhang, Xuyang Zhu, Zhengbao Zha, Haisheng Qian, Liang Cheng, Xianwen Wang
Journal: Biomaterials (2022)
Endothelial <i>Rbpj</i> deletion normalizes Notch4-induced brain arteriovenous malformation in mice
Authors: Corinne M. Nielsen, Xuetao Zhang, Kunal Raygor, Shaoxun Wang, Andrew W. Bollen, Rong A. Wang
Journal: The Journal of Experimental Medicine (2022)

Upregulation of Notch signaling is associated with brain arteriovenous malformation (bAVM), a disease that lacks pharmacological treatments. Tetracycline (tet)-regulatable endothelial expression of constitutively active Notch4 (Notch4*tetEC) from birth induced bAVMs in 100% of mice by P16. To test whether targeting downstream signaling, while sustaining the causal Notch4*tetEC expression, induces AVM normalization, we deleted Rbpj, a mediator of Notch signaling, in endothelium from P16, by combining tet-repressible Notch4*tetEC with tamoxifen-inducible Rbpj deletion. Established pathologies, including AV connection diameter, AV shunting, vessel tortuosity, intracerebral hemorrhage, tissue hypoxia, life expectancy, and arterial marker expression were improved, compared with Notch4*tetEC mice without Rbpj deletion. Similarly, Rbpj deletion from P21 induced advanced bAVM regression. After complete AVM normalization induced by repression of Notch4*tetEC, virtually no bAVM relapsed, despite Notch4*tetEC re-expression in adults. Thus, inhibition of endothelial Rbpj halted Notch4*tetEC bAVM progression, normalized bAVM abnormalities, and restored microcirculation, providing proof of concept for targeting a downstream mediator to treat AVM pathologies despite a sustained causal molecular lesion.
Neutralizing antibodies induced by homologous and heterologous boosters in CoronaVac vaccines in Chile
Authors: Johanna Acevedo, Mónica L. Acevedo, Aracelly Gaete-Argel, Rafael Araos, Cecilia Gonzalez, Daniela Espinoza, Solange Rivas, Pablo Pizarro, Stephan Jarpa, Ricardo Soto-Rifo, Alejandro Jara, Fernando Valiente-Echeverría
Journal: Clinical Microbiology and Infection (2022)

To determine the impact of a booster dose on the humoral response in individuals inoculated with a complete schedule of any SARS-CoV-2 vaccine, we evaluated the neutralizing antibody (NAb) titres of homologous or heterologous booster doses over a 90-days period in CoronaVac vaccinees from 3 centres in Santiago, Chile.Individuals previously inoculated with 2 doses of CoronaVac (N = 523) were recruited in the context of the REFUERZO clinical trial (NCT04992182) and received either placebo (N = 129), or a booster dose of CoronaVac (N = 134), BNT162b2 (N = 133), or ChAdOx1 (N = 127). Pseudovirus neutralizing antibody titres (pVNT) were determined at baseline (day 0) as well as at days 14, 30, 60, and 90 after booster dose administration.Inoculating a booster dose increases the pVNTs titres at days 14 and 30 in all groups, (13.5- and 12.0-fold increase for the CoronaVac group; 247.0- and 212.3-fold increase for the BTN162b2 group; and 89.1- and 128.1-fold increase for ChAdOx1 at each time point, respectively) with a decline observed at days 60 and 90. However, although pVNTs remained significantly higher for the BTN162b2 and ChAdOx1 groups at days 60 and 90, NAb titres reached baseline levels in the CoronaVac group at 90 days after inoculation.A single heterologous booster (BTN162b2 or ChAdOx1) in individuals who completed the CoronaVac primary series resulted in an important increase in NAb titres remaining significantly higher at least for 90 days. These data may directly impact middle- and low-income countries currently using CoronaVac as the main vaccination strategy.
Corynebacterium ulcerans as filamentous branching rods
Authors: Claudie Lamoureux, Schéhérazade Rézig, Hervé Le Bars, Felipe Le Divenah, Didier Tandé, Lourdes Vélo-Suarez, Edgar Badell, Sylvain Brisse, Geneviève Héry-Arnaud, Clémence Beauruelle
Journal: Clinical Microbiology and Infection (2022)
Innovations to reduce maternal mortality and improve health and wellbeing of adolescent girls and their babies in Sierra Leone
Authors: Cristina Fernandez Turienzo, Lucy November, Mangenda Kamara, Philemon Kamara, Venetia Goodhart, Alexandra Ridout, Betty Sam, Suzanne Thomas, Prince T Williams, Jane Sandall, Andrew H Shennan
Journal: The Lancet Child & Adolescent Health (2022)
Advancing drug delivery to articular cartilage: From single to multiple strategies
Authors: Tianyuan Zhao, Xu Li, Hao Li, Haoyuan Deng, Jianwei Li, Zhen Yang, Songlin He, Shuangpeng Jiang, Xiang Sui, Quanyi Guo, Shuyun Liu
Journal: Acta Pharmaceutica Sinica B (2022)
A redox-responsive self-assembling COA-4-arm PEG prodrug nanosystem for dual drug delivery suppresses cancer metastasis and drug resistance by downregulating hsp90 expression
Authors: Yi Zhou, Yingling Miao, Qiudi Huang, Wenwen Shi, Jiacui Xie, Jiachang Lin, Pei Huang, Chengfeng Yue, Yuan Qin, Xiyong Yu, He Wang, Linghao Qin, Jianhai Chen
Journal: Acta Pharmaceutica Sinica B (2022)

Metastasis and resistance are main causes to affect the outcome of the current anticancer therapies. Heat shock protein 90 (Hsp90) as an ATP-dependent molecular chaperone takes important role in the tumor metastasis and resistance. Targeting Hsp90 and downregulating its expression show promising in inhibiting tumor metastasis and resistance. In this study, a redox-responsive dual-drug nanocarrier was constructed for the effective delivery of a commonly used chemotherapeutic drug PTX, and a COA-modified 4-arm PEG polymer (4PSC) was synthesized. COA, an active component in oleanolic acid that exerts strong antitumor activity by downregulating Hsp90 expression, was used as a structural and functional element to endow 4PSC with redox responsiveness and Hsp90 inhibitory activity. Our results showed that 4PSC/PTX nanomicelles efficiently delivered PTX and COA to tumor locations without inducing systemic toxicity. By blocking the Hsp90 signaling pathway, 4PSC significantly enhanced the antitumor effect of PTX, inhibiting tumor proliferation and invasiveness as well as chemotherapy-induced resistance in vitro. Remarkable results were further confirmed in vivo with two preclinical tumor models. These findings demonstrate that the COA-modified 4PSC drug delivery nanosystem provides a potential platform for enhancing the efficacy of chemotherapies.
Protection against symptomatic infection with delta (B.1.617.2) and omicron (B.1.1.529) BA.1 and BA.2 SARS-CoV-2 variants after previous infection and vaccination in adolescents in England, August, 2021–March, 2022: a national, observational, test-negative, case-control study
Authors: Annabel A Powell, Freja Kirsebom, Julia Stowe, Mary E Ramsay, Jamie Lopez-Bernal, Nick Andrews, Shamez N Ladhani
Journal: The Lancet Infectious Diseases (2022)
Signaling pathways in cancer‐associated fibroblasts: recent advances and future perspectives
Authors: Zengli Fang, Qingcai Meng, Jin Xu, Wei Wang, Bo Zhang, Jiang Liu, Chen Liang, Jie Hua, Yingjun Zhao, Xianjun Yu, Si Shi
Journal: Cancer Communications (2022)

As a critical component of the tumor microenvironment (TME), cancer-associated fibroblasts (CAFs) play important roles in cancer initiation and progression. Well-known signaling pathways, including the transforming growth factor-β (TGF-β), Hedgehog (Hh), Notch, Wnt, Hippo, nuclear factor kappa-B (NF-κB), Janus kinase (JAK)/signal transducer and activator of transcription (STAT), mitogen-activated protein kinase (MAPK), and phosphoinositide 3-kinase (PI3K)/AKT pathways, as well as transcription factors, including hypoxia-inducible factor (HIF), heat shock transcription factor 1 (HSF1), P53, Snail, and Twist, constitute complex regulatory networks in the TME to modulate the formation, activation, heterogeneity, metabolic characteristics and malignant phenotype of CAFs. Activated CAFs remodel the TME and influence the malignant biological processes of cancer cells by altering the transcriptional and secretory characteristics, and this modulation partially depends on the regulation of signaling cascades. The results of preclinical and clinical trials indicated that therapies targeting signaling pathways in CAFs demonstrated promising efficacy but were also accompanied by some failures (e.g., NCT01130142 and NCT01064622). Hence, a comprehensive understanding of the signaling cascades in CAFs might help us better understand the roles of CAFs and the TME in cancer progression and may facilitate the development of more efficient and safer stroma-targeted cancer therapies. Here, we review recent advances in studies of signaling pathways in CAFs and briefly discuss some future perspectives on CAF research.
Characterisation of a high-risk profile for maternal thrombotic and severe haemorrhagic complications in pregnant women with antiphospholipid syndrome in France (GR2): a multicentre, prospective, observational study
Authors: Anne Murarasu, Gaëlle Guettrot-Imbert, Véronique Le Guern, Cécile Yelnik, Viviane Queyrel, Nicolas Schleinitz, Nicole Ferreira-Maldent, Elisabeth Diot, Geoffrey Urbanski, Emmanuelle Pannier, Estibaliz Lazaro, Odile Souchaud-Debouverie, Pauline Orquevaux, Nicolas Belhomme, Nathalie Morel, Elodie Chauvet, François Maurier, Maëlle Le Besnerais, Noemie Abisror, Tiphaine Goulenok, Françoise Sarrot-Reynauld, Alban Deroux, Elisabeth Pasquier, Claire de Moreuil, Holy Bezanahary, Laurent Pérard, Nicolas Limal, Vincent Langlois, Anne Calas, Bertrand Godeau, Christian Lavigne, Eric Hachulla, Fleur Cohen, Ygal Benhamou, Loïc Raffray, Mathilde de Menthon, Nathalie Tieulié, Vincent Poindron, Luc Mouthon, Maddalena Larosa, Elisabeth Eléfant, Loic Sentilhes, Anna Molto, Catherine Deneux-Tharaux, Nathalie Costedoat-Chalumeau, Emmanuel Azzi, Béatrice Banneville, Antoine Baudet, Constance Beaudouin-Bazire, Cristina Belizna, Rakiba Belkhir, Alice Berezne, Emilie Berthoux, Sabine Berthier, Lisa Biale, Boris Bienvenu, Claire Blanchard-Delaunay, Pascal Cathebras, Claire Cazalets, Benjamin Chaigne, Olivia Chandesris, Jérémy Chatelais, Emmanuel Chatelus, Pascal Coquerelle, Marion Couderc, Juliette Delforge, Amélie Denis, Sandra Desouches, Philippe Dieudé, Guillaume Direz, Marine Driessen, Aurélie Du Thanh, Laetitia Dunogeant, Cécile Durant, Isabelle Durieu, Marc Fabre, Olivier Fain, René-Marc Flipo, Aline Frazier, Antoine Froissart, Sophie Georgin-Lavialle, Elisabeth Gervais, Anne Gompel, Laure Gossec, Phillipe Goupille, Claire Grange, Constance Guillaud-Danis, Aurélie Hummel, Moez Jallouli, Patrick Jego, Stéphane Jobard, Laurence Josselin-Mahr, Noémie Jourde-Chiche, Anne-Sophie Korganow, Marc Lambert, Delphine Lariviere, Claire Larroche, Céline Lartigau-Roussin, Augustin Latourte, Thomas Le Gallou, Gaëlle Leroux, Hervé Levesque, Frédéric Lioté, Jonathan London, Valentine Loustau, Emmanuel Maheu, Matthieu Mahevas, Hélène Maillard, Xavier Mariette, Hubert Marotte, Nicolas Martin-Silva, Nihal Martis, Agathe Masseau, Arsène Mekinian, Sara Melboucy-Belkhir, Martin Michaud, Marc Michel, Chafika Morati-Hafsaoui, Jacky Nizard, Jérémy Ora, Jean-Loup Pennaforte, Antoinette Perlat, Hélène Petit Bauer, Evangeline Pillebout, Jean-Maxime Piot, Agnès Portier, Gregory Pugnet, Manon Redondin, Alexis Regent, Christophe Richez, Mélanie Roriz, Laurent Sailler, Gaëtan Sauvêtre, Léa Savey, Vincent Sobanski, Christelle Sordet, Martin Soubrier, Katia Stankovic Stojanovic, Thierry Thomas, Marie-Agnès Timsit, Vassilis Tsatsaris
Journal: The Lancet Rheumatology (2022)